Distinct epidermal keratinocytes respond to extremely low-frequency electromagnetic fields differently

PLoS One. 2014 Nov 19;9(11):e113424. doi: 10.1371/journal.pone.0113424. eCollection 2014.

Abstract

Following an increase in the use of electric appliances that can generate 50 or 60 Hz electromagnetic fields, concerns have intensified regarding the biological effects of extremely low-frequency electromagnetic fields (ELF-EMFs) on human health. Previous epidemiological studies have suggested the carcinogenic potential of environmental exposure to ELF-EMFs, specifically at 50 or 60 Hz. However, the biological mechanism facilitating the effects of ELF-EMFs remains unclear. Cellular studies have yielded inconsistent results regarding the biological effects of ELF-EMFs. The inconsistent results might have been due to diverse cell types. In our previous study, we indicated that 1.5 mT, 60 Hz ELF-EMFs will cause G1 arrest through the activation of the ATM-Chk2-p21 pathway in human keratinocyte HaCaT cells. The aim of the current study was to investigate whether ELF-EMFs cause similar effects in a distinct epidermal keratinocyte, primary normal human epidermal keratinocytes (NHEK), by using the same ELF-EMF exposure system and experimental design. We observed that ELF-EMFs exerted no effects on cell growth, cell proliferation, cell cycle distribution, and the activation of ATM signaling pathway in NHEK cells. We demonstrated that the 2 epidermal keratinocytes responded to ELF-EMFs differently. To further validate this finding, we simultaneously exposed the NHEK and HaCaT cells to ELF-EMFs in the same incubator for 168 h and observed the cell growths. The simultaneous exposure of the two cell types results showed that the NHEK and HaCaT cells exhibited distinct responses to ELF-EMFs. Thus, we confirmed that the biological effects of ELF-EMFs in epidermal keratinocytes are cell type specific. Our findings may partially explain the inconsistent results of previous studies when comparing results across various experimental models.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins / metabolism
  • Cell Proliferation / radiation effects
  • Cells, Cultured
  • Checkpoint Kinase 2 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Electromagnetic Fields*
  • Epidermal Cells
  • G1 Phase Cell Cycle Checkpoints / radiation effects
  • Humans
  • Hydrogen Peroxide / toxicity
  • Keratinocytes / cytology
  • Keratinocytes / metabolism
  • Keratinocytes / radiation effects*
  • Phosphorylation / drug effects
  • Signal Transduction / radiation effects
  • Ultraviolet Rays

Substances

  • Cyclin-Dependent Kinase Inhibitor p21
  • Hydrogen Peroxide
  • Checkpoint Kinase 2
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • CHEK2 protein, human

Grants and funding

The authors would like to thank the National Science Council, Taiwan, for supporting this research financially under Contract (Grant number: NSC 101-2112-M-007-003-MY3, http://web1.most.gov.tw/). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.